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. 2017 Oct 30;12:29. doi: 10.1186/s12263-017-0581-3

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© The Author(s) 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — A general diagram showing the physiological basis responsible for the NPC1 gene-nutrient interaction that promotes weight gain and susceptibility to obesity. Mouse model tissues (liver and adipose) and fibroblasts grown in culture indicate (i) increased glycolysis (oxidation of glucose and conversion to pyruvate in the cytoplasm), (ii) decreased oxidative metabolism (conversion of pyruvate to acetyl-CoA and condensation with oxaloacetate to produce citrate in the mitochondria), (iii) increased lipogenesis pathway (transport of citrate from the mitochondria and conversion to acetyl-CoA and malonyl-CoA for lipid (cholesterol and fatty acid) synthesis in the cytoplasm), and (iv) decreased lipolysis pathway (transport of fatty acid from the cytoplasm and conversion of fatty acid to acetyl-CoA in the mitochondria)